Two forms of human alcoholic myopathy can be defined: 1. Rapid onset of weakness, rhabdomyolysis, and myoglobinuria often resulting in acute renal tubular necrosis. 2. Subclinical myopathy manifested by high CPK (50 percent) and minor, non-specific morphologic changes on muscle biopsy. We have not found clinical evidence of a chronic, progressive myopathy. Both normal controls and chronic alcoholics exposed to ethanol fail to generate normal amounts of lactic acid when exercising. We feel this is due to the use of energy sources other than glycogen during alcohol exposure. Alcoholics differ from controls, however, in that this depression of lactate production may persist for several days after acute ethanol exposure. The reason for this is unclear and is being explored. Acute alcohol exposure does not result in any major or dramatic alteration in the level of phosphorylated intermediates in muscle. Acute exposure also has remarkably little effect on the mechanical properties of muscle. The programmed feeding model for producing chronic alcoholism in the rat is most reliable and highly effective. Chronic alcohol exposure in the otherwise normal rat produces little morphologic change in muscle. Hypokalemia appears to be an important factor in the muscle damage produced by ethanol.